Switching to IgE can be activated by a combination of IL4, which induces transcription in that region, and anti-CD40 antibody, which induces cell proliferation. We have decided to dissect the process first using the human CL-01 B cell line, which we have shown to respond appropriately to IL4. IL4 causes a 100X increase in transcript, both unspliced and spliced over the IgE switch region on induction. We also observed a sizable (5X) increase transcription of AID, the cytidine deaminase that is responsible for initiating CSR. This is similar to effects observed in primary B cells. [unreadable] We have surveyed a battery of histone modifications at high resolution in uninduced and induced CL-01 cells, focusing on the region between the I-epsilon promoter and the 3 end of the IgE switch region, the most important region associated with this CSR event. These modifications included histone H3 acetylation at both K9 and K14 or K9 alone; histone H4 tetra-acetylation (K5/8/12/16), H3 K4 dimethylation, and H3 K27 trimethylation. Either acetyl-H3K9/14 or acetyl-H3K9 alone showed marked increases on induction. All other modifications were not greatly changed between uninduced and induced cells. However the distribution of a given modification over the region was in most cases non-uniform: for example, dimethyl-H3K4, tetraacetyl-H4, and acetyl-H3 K9/14 all showed relative peaks over the I-epsilon promoter. To interpret these results the abundance of nucleosomes was mapped across the same region, and a relative depletion over I-epsilon was observed. No change in the nucleosome abundance was observed on induction. We are now extending these observations to studying the distribution of the histone variants H3.3 and H2A.Z, and also investigating the same modifications after induction of primary B cells.